CORTISONE, the first of the adrenocortical steroids with glucocorticoid and mineralocorticoid actions, was demonstrated in 1949 by Hench and his colleagues as being of use in the treatment of rheumatoid arthritis. Very soon its therapeutic horizon was widely extended to cover a large number of other conditions, mostly endocrinological or inflammatory. After this, hydrocortisone (cortisol) appeared, then prednisolone and prednisone, triamcinolone, methyl prednisolone and, finally, dexamethasone. Each was brought out in the hope that side (unwanted) effects would be less while clinical (wanted) effects would be more, and claims were made for each in turn which later work failed to confirm in all instances. All compounds produced since hydrocortisone had demonstrably less sodiumretaining effect: triamcinolone differed from the others in producing a certain number of side-effects not common with its predecessors, anorexia instead of the usual tonic effect on the appetite, post-prandial flushing, giddiness and, the most important, myasthenia. Ten years after the original cortisone was produced from the laboratories of Merck & Co. in New Jersey, their new substance appeared, dexamethasone (Decadron, Merck Sharp & Doh me). The claims were that this new substance was far more potent than any of its predecessors and that it (once again, almost, one might say, inevitably) produced fewer "side" effects.One point should be emphasized here. These so-called side effects are very much intrinsic, built-in properties of the drug. Cortisone, a hormone, when given in pharmacological doses to patients with intact adrenal glands, produces, inevitably, some of the features of Cushing's disease: striae, acne, ecchymoses, moon face, overgrowth of fluffy, fine hair, osteoporosis and, occasionally, fractures, mental upsets, peptic u,Jceration, glycosuria and hyperglycaemia. So, in fact, do all